Identity and topographic localization of immunocompetent cells and alteration of surface markers on ocular resident cells in rodents with experimental autoimmune uveoretinitis (EAU) were analyzed by immunohistochemical studies. In the early stage of EAU, T helper/inducers were the predominant cells in the eye; in the late stage, a relative increase of T suppressor/cytotoxic cells was observed. T lymphocyte specificity is directed to small fragments of antigen bound to cell surface major histocompatibility complex (MHC) molecules which are presented on the surface of specialized antigen-presenting cells. Expression of MHC class II antigens was observed on ocular resident cells such as RPE, retinal endothelium, keratocytes, fibroblasts, and ciliary epithelium. Both the infiltrating cell subpopulation and the expression of class II antigens on ocular resident cells can be altered by various immunomodulating agents, some of which-Qingaining, FK506, 15-deoxyspergualine, interleukin 2-PE40, and S-antigen-were evaluated for their immunopathological effects on EAU. Clinical and immunopathologic examinations of the eyes of mice with EAU demonstrated a chronic relapsing focal granulomatous inflammation and vasculitis in the retina and choroid. Development of subretinal neovascularization may also occur. The infiltrating cells were mainly macrophages and T helpers/inducers (CD4). The expression of MHC class II antigens is confined to ocular resident cells immediately at the inflammatory sites. Due to the chronicity and recurrence of EAU, the mouse may serve as a better model for human ocular inflammation. Experimental endotoxin-induced uveitis (EIU) is a model for anterior uveitis in humans. The mechanism of this inflammation is still unclear. Because recently it has been suggested that activation of phospholipase A2 may play a role in the initiation and propagation of this disease, we studied the effect of a novel synthetic peptide and a PLA2 inhibitor, antiflammin, on EIU in rats.